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Erschienen in:
01.10.2013 | What's New in Intensive Care
Endothelial injury in sepsis
Erschienen in: Intensive Care Medicine | Ausgabe 10/2013
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Vascular endothelial cells play a pivotal mediatory role in many responses to systemic inflammation including the crosstalk between coagulation and inflammation in sepsis [1, 2]. Endothelial cells respond to the cytokines expressed and released by activated leukocytes but can also release cytokines themselves. Furthermore, endothelial cells are able to express adhesion molecules and growth factors that may not only promote the inflammatory response further but also affect a myriad of downstream responses. It has recently become clear that, in addition to these mostly indirect effects of the endothelium, injured endothelial cells directly interfere with platelet–vessel wall interaction, neutrophil entrapment through formation of extracellular nets, and activation of inflammation and coagulation mediated by microparticles (Fig. 1).
Fig. 1
Schematic representation of interaction between several cells and (injured) endothelium in sepsis and its consequences. Activated inflammatory cells adhere to endothelial cells through binding to specific receptors and entrapment within neutrophil extracellular traps (NETs) and may induce expression of tissue factor that activates platelets and the coagulation system. Activated platelets promote further tissue factor expression through P-selectin. Platelets bind to endothelium via ultralarge von Willebrand factor multimers, which are insufficiently cleaved due to a relative insufficiency of its cleaving protease, ADAMTS13. Activated coagulation proteases bind to protease-activated receptors (PARs), which may induce additional proinflammatory stimuli by releasing cytokines that target endothelial cells and mononuclear cells
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